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Stearoyl-CoA desaturase (SCD) is conserved in all eukaryotes and introduces the first double bond into saturated fatty acyl-CoAs. Because the monounsaturated products of SCD are key precursors of membrane phospholipids, cholesterol esters and triglycerides, SCD is pivotal in fatty acid metabolism. Humans have two SCD homologues (SCD1 and SCD5), while mice have four (SCD1–SCD4).

Background

An overview of stearoyl-CoA Desaturase (SCD)

Stearoyl-CoA Desaturase (SCD), a member of the dehydrogenase family, is highly conserved in the evolution of animals, plants and yeast. It is also a speed-limiting enzyme in the synthesis of fatty acids.

Major types of stearoyl-CoA Desaturase (SCD)

Mammalian SCDs are divided into five subtypes, of which are four subtypes of mouse SCD (SCD-1~SCD4), two subtypes of human SCD (SCD-1 and SCD-5), and two subtypes of bovine SCD (SCD-1 and SCD-5). In addition, the corresponding SCD gene was also found in sheep, pigs and chicken.

Inhibition of stearoyl-CoA Desaturase (SCD)

A939572 is a small molecule that specifically inhibits the activity of SCD-1. In vitro, A939572 decreases the effect and shows strong body activity, depending on the dose-dependent saturation index. A939572 shows a significant decrease in the proliferation of Caki1, A498, Caki2 and Achn in 5 days (respectively 65 nM、50 nM、65 nM and 6 nM). In vivo, A939572 and Tem single drugs produce similar growth responses, about 20-30% reduce tumor volume (vs. placebo control).

Stearoyl-CoA Desaturase (SCD) and diseases

In order to adapt to the rapid development of modern life, reduced physical activity and increased energy intake has led to the onset of obesity , and obesity exacerbated diabetes, coronary artery disease, high blood pressure and nonalcoholic fatty liver diseases. The occurrence of these diseases is related to the lipid distribution in the cells, and SCD-1 is proposed as a potential means of treating obesity and metabolic syndrome. The expression level of SCD-1 in obese mouse model is high, which shows the phenotype of liver fat metamorphosis and insulin resistance. Conversely, in the SCD-1-deficient mouse model, it is sensitive to insulin. In addition, high triglyceride is associated with increased activity of SCD1. Further studies have shown that the increase of SCD-activity can inhibit ABCA1-mediated alcohol output, while SCD1 deficiency reduces the synthesis level of VLDL in obese mouse. Also, a large number of studies have confirmed that SCD-1 is the key to lipid homeostasis and weight control, revealing the prospect of SCD-1 as a therapeutic tool for obesity and other metabolic syndromes.